The Response of Renal Tubular Epithelial Cells to Physiologically and Chemically Induced Growth Arrest

Jeong, Jeongmi K.; Huang, Qihong; Lau, Serrine S.; Monks, Terrence J.

doi:10.1074/jbc.272.11.7511

Cited by 19 publications

(20 citation statements)

References 56 publications

(44 reference statements)

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“…p53 is a zinc finger transcription factor that induces the transcription of a variety of proteins including p21, Gadd45, and Gaddl53 (50,51), which are involved in cell cycle arrest and DNA repair. Transcription of p53 is inhibited by adenovirus E 1 B protein (103), Epstein-Barr virus E6 proteins (138), WT 1 expression (81), bcl-2 (13), and bfl (19).…”

Section: P53mentioning

confidence: 99%

Review Article: Apoptosis in the Kidney

Davis

Ryan

1998

Toxicol Pathol

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Apoptosis is a highly regulated mechanism of cell death. Although apoptosis has a functional role in normal development and tissue homeostasis, aberrant triggering of the process by toxicants may lead to abnormal function or disease. Low level exposures to toxicants that induce apoptosis in kidney may therefore create a critical disturbance in kidney homeostasis, contributing to renal neoplasia or renal disease. In this report, we review the involvement of apoptosis in normal kidney development and in renal disease and discuss some of the toxicants and molecular factors involved in regulation of the process in renal cells.

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Section: P53mentioning

confidence: 99%

Review Article: Apoptosis in the Kidney

Davis

Ryan

1998

Toxicol Pathol

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“…One such gene, Gadd153 (also known as chop), encodes a member of the CCAAT\enhancer-binding protein (C\EBP) family of transcription factors. Originally isolated based on its induction by UV-C irradiation [1], Gadd153 has subsequently been shown to be highly induced in a variety of stress paradigms that result in growth arrest or DNA damage, including genotoxic agents [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16], calcium ionophore [17], nutrient depletion [15,[18][19][20], oxidative stress [21][22][23], reductive stress [24,25], endoplasmic reticulum stress [26][27][28] and the acute-phase response [29,30]. GADD153 (where GADD stands for growth arrest and DNA damage-inducible protein) has been implicated in the commitment to, or implementation of, growth arrest or cell death ; microinjection of GADD153 induces 3T3 cells to arrest at the G " \S boundary [31], while ectopic expression of GADD153 causes M1 myeloblastic leukaemia cells to undergo apoptosis [32].…”

Section: Introductionmentioning

confidence: 99%

Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)–ATF composite site to regulate Gadd153 expression during the stress response

Fawcett

Martindale

Guyton

et al. 1999

Biochemical Journal

375

229

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Gadd153, also known as chop, encodes a member of the CCAAT/enhancer-binding protein (C/EBP) transcription factor family and is transcriptionally activated by cellular stress signals. We recently demonstrated that arsenite treatment of rat pheochromocytoma PC12 cells results in the biphasic induction of Gadd153 mRNA expression, controlled in part through binding of C/EBPβ and two uncharacterized protein complexes to the C/EBP–ATF (activating transcription factor) composite site in the Gadd153 promoter. In this report, we identified components of these additional complexes as two ATF/CREB (cAMP-responsive-element-binding protein) transcription factors having differential binding activities dependent upon the time of arsenite exposure. During arsenite treatment of PC12 cells, we observed enhanced binding of ATF4 to the C/EBP–ATF site at 2 h as Gadd153 mRNA levels increased, and enhanced binding of ATF3 complexes at 6 h as Gadd153 expression declined. We further demonstrated that ATF4 activates, while ATF3 represses, Gadd153 promoter activity through the C/EBP–ATF site. ATF3 also repressed ATF4-mediated transactivation and arsenite-induced activation of the Gadd153 promoter. Our results suggest that numerous members of the ATF/CREB family are involved in the cellular stress response, and that regulation of stress-induced biphasic Gadd153 expression in PC12 cells involves the ordered, sequential binding of multiple transcription factor complexes to the C/EBP–ATF composite site.

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“…LLC-PK 1 cells cultured in a growth factor-deprived medium enter quiescence within 48 h [21], as shown in Fig. 1A (empty columns).…”

Section: Bmmc and Msc Stimulate Renal Epithelial Cell Proliferationmentioning

confidence: 93%

Paracrine Interaction between Bone Marrow-derived Stem Cells and Renal Epithelial Cells

Lindoso

Araujo

Adão-Novaes

et al. 2011

Cell Physiol Biochem

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Background/Aims: Renal tubular cells are the main target of ischemic insult associated with acute renal injury. Low oxygen and nutrient supplies result in ATP depletion, leading to cell death and loss of renal function. A possible mechanism by which bone marrow-derived cells support renal tissue regeneration relies on the capacity of mononuclear cells (BMMC), particularly mesenchymal stem cells (MSC), to secrete paracrine factors that mediate support for kidney regeneration. Methods: BMMC/MSC and renal cells (LLC-PK₁ from pig and IRPTC from rat) were co-cultured under stressful conditions (ATP depletion and/or serum free starvation), physically separated by a microporous membrane (0.4 µm), was used to determine whether bone marrow-derived cells can interact with renal cells in a paracrine manner. Results: This interaction resulted in stimulation of renal cell proliferation and the arrest of cell death. MSC elicit effective responses in renal cells in terms of stimulating proliferation and protection. Such effects are observed in renal cells co-cultured with rat BMMC/MSC, an indication that paracrine mechanisms are not entirely species-specific. Conclusion: The paracrine action of BMMC/MSC was influenced by a renal cell stimulus released during stress, indicating that cross-talk with injured cells is required for renal regeneration supported by bone marrow-derived cells.

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The Response of Renal Tubular Epithelial Cells to Physiologically and Chemically Induced Growth Arrest

Cited by 19 publications

References 56 publications

Review Article: Apoptosis in the Kidney

Review Article: Apoptosis in the Kidney

Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)–ATF composite site to regulate Gadd153 expression during the stress response

Paracrine Interaction between Bone Marrow-derived Stem Cells and Renal Epithelial Cells

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